TUBERCULOSIS

Dr. Shaswat Bhattarai

1st year JR, Pathology
 WHAT IS IT?
 Bacterial infection

 Caused by Mycobacterium tuberculosis (also

called tubercle bacillus)

 Damages a person’s lungs or other parts of

the body

 Fatal if not treated properly

• Mycobacterium – Slender, aerobic rods
Gram +ve, Acid fast

M.tuberculosis – Reservoir- Humans

M.bovis –Reservoir – contaminated milk

M.Avium intracellulare-opportunistic
(AIDS)
TB flourishes in

 Poverty, Over crowding, Malnutrition

 DM

 Alcoholism

 Immunosuppression
 TRANSMISSION
• Spreads through the air when a
person with active TB (Inhalation)

– Coughs

– Speaks

– Laughs

– Sneezes

• Ingestion
 SPREAD OF TB
 Local Spread

 Lymphatic spread

 Haematogenous Spread

 Natural passages – Pleurisy,

Peritonitis (salpingitis), Laryngitis ,
Ileocaecal
 PATHOGENESIS

• Breath in infected air and bacilli go to lungs

through bronchioles

• Bacilli infect alveoli

• Macrophages attack bacteria, but some

survive

• Infected macrophages separate and form

tubercles
Hypersensitivity to tubercular antigens

Cell Mediated immunity

Caseating granulomas, Cavitation

Host response to lipids such as Mycosides

(cord factor) & glycolipids ( Wax-D) on the

bacterial cell wall

Type IV Hypersensitivity
Primary cells infected
are

MACROPHAGES
ACTIVE INFECTION

Unhealthy person

Bacilli overwhelm immune system

Bacilli break out of tubercles in alveoli

and spread through
bloodstream
LATENT INFECTION

Initial infection controlled

by immune system

Bacilli remain confined in

tubercles for years
 DIAGNOSIS

• Mantoux test
Positive > 15mm
• Medical history,
x-rays, and smears for
AFB, Sputum culture,
PCR
 SYMPTOMS
• Perpetual Cough

• Fever

• Weight loss

• Night sweats

• Loss of appetite

• Fatigue

• Swollen glands

• Pain while breathing

EVOLUTION OF TUBERCLE ( Granuloma)
PMN

Macrophages

Poorly degradable bacilli

CD4+ T cells
( IFN, TNF)
Epithelioid cells

Hard Tubercle

Soft Tubercle
GRANULOMA

Central caseous necrosis surrounded by

epithelioid cells, Langhan’s giant cells,

Rim of lymphocytes and fibroblasts.

FATE OF GRANULOMA

Cold Abscess

Sinus Formation

Fibrosis

Dystrophic calcification
CLINICAL SPECTRUM

 Primary – previously unexposed, unsensitized

person.

 Secondary – Previously sensitized person

- Follows primary,

- Reactivation of dormant lesion,

- Exogenous reinfection ( Large

inoculum of virulent bacilli)

 Primary tuberculosis
GHON’S COMPLEX( Primary complex)

 Ghon’s Focus- Subpleural focus in the

upper part of lower lobe/
lower part of upper lobe
 Lymphatic component
 Lymph node component – Hilar &
Tracheo-bronchial
Fate of Primary TB

 Fibrosis, calcification

 Progressive Pulmonary TB

 Primary Miliary TB

 Secondary TB
Secondary Tuberculosis

 Initially -- small focus (2 cm) of

consolidation in the apical pleura

 Develop a small area of caseation, fibrosis

Fate of secondary TB

 Heal with fibrosis

 Fibrocavitary TB

 Pneumonia

 Miliary TB
Progressive Pulmonary TB

 Child, Elderly, Immunocompromised

 Erosion of blood vessels hemoptysis

 Erosion into bronchus

 Empyema, effusion, pleuritis

MILIARY TUBERCULOSIS

 Miliary = ‘millet seeds’

 Spread thro’ lymphatics

 Lesions- small / microscopic

 Liver, Spleen, Kidney, Brain, Bonemarrow

adrenals, fallopian tubes, epididymis, etc.
Isolated organ TB:

• Meningitis
• Renal
• Osteomyelitis
• Adrenals
• Salpingitis
• Pott’s spine
• Lymphadenitis- Scrofula
• Intestinal
 IMMUNIZATION

Bacilli Calmette Guerin ( BCG)

[ Attenuated Strains of Bovine type of Bacilli]
THANK YOU